Heretofore, circulatory disturbances exhibiting causally or symptomatically different syndromes have been treated with drugs having specific actions in each case. Circulatory disturbances as general indications of illness are caused, in the view generally held today, on the one hand, by arteriosclerotic constrictions of the blood vessels and, on the other hand, by pathological changes of the blood flow properties, the restricted microcirculation resulting in a deficient blood supply of the tissue.
In general, circulatory disturbances are often accompanied by a restriction of the functionality of all tissues and organ systems. The functions of the heart, brain, eyes, inner ear and muscle tissue, and particularly of the extremities, are especially affected. Diseases of the coronary vessels which can lead, for instance, to myocardial infarction and sudden heart death, such as angina pectoris, are caused, on the one hand, by arteriosclerosis and spasms and, on the other hand, by hypertension combined with an impairment of the blood flow properties. This generally results in a lack of substrate and oxygen. In general, the identical pathogenetic principle applies to circulatory disturbances of the eye, the inner ear and the muscle tissue, the microcirculation being debilitated due to the impaired fluidity of the blood. K. U. Benner, GIT Labor Medizin, 5, 295-302 1985.
According to the modern view, the following clinical pictures result from the interaction between the morphologically modified blood vessel and the pathologically modified blood vessel and the pathologically modified content of the vessel, namely, liquid components (plasma) and corpuscular components (erythrocytes and thrombocytes or platelets). Diseases of the brain include: transitory ischemic attacks (TIA), PRIND (prolonged reversible ischemic neurological deficits), COP (cerebral organic psychosyndrome) with functional deficits all the way to cerebral infarction (apoplexy). Diseases of the vessels include: coronary heart disease, angina pectoris as well as hypertension. The latter is in itself combined with impaired blood flow properties and is additionally considered as risk factor for apoplexy and myocardial infarction. Diseases of the muscles include: intermittent claudication, ulcus cruris, gangrene all the way to necrosis resulting in amputation, and Raynaud's disease. In the eye, the consequences include impaired vision, all the way to blindness. In the ear, the consequences include tinnitus, hearing impairment and sudden decline in hearing including total loss of hearing.
Dihydropyridines having calcium-antagonist effect of the formula: ##STR3## in which R.sub.1 is a CH.sub.3 --O--CH.sub.2 --CH.sub.2 --or--CH.sub.3 group; R.sub.2 is a ##STR4## or CH.sub.3 --CH.sub.2 --group; R.sub.3 is H, NO.sub.2 or Cl; and R.sub.4 is NO.sub.2, H or Cl and pharmaceutically acceptable salts thereof; and particularly Nifedipine, Nimodipine, Nitrendipine, Nicardipine and Felodipine are known and used in the treatment of coronary heart diseases (CHD) and/or high blood pressure (hypertension). The effectiveness, particularly in the case of CHD, hypertension and spastic conditions of the smooth muscles, for instance in the case of asthma, spasms of the uterus, etc., of the above mentioned dihydropyridines is based on their selective inhibition of the calcium influx through the cell membrane of the smooth muscles of the vessels, including the coronary vessels, without affecting the concentration of calcium ions in the blood serum See A. Fleckenstein, H. Roskamm, "Calcium-Antagonismus", Springer-Verlag, 1980.
Pentoxifylline is known and described in Federal Republic of Germany Pat. No. 12 35 320. Pentoxifylline is used for treating disturbances of the peripheral and cerebral circulation. It has no pronounced hemodynamic (affecting the blood) or spasmolytic action such as, for instance, the aforementioned dihydropyridines. Pentoxifylline primarily improves the erythrocyte flexibility, reduces the tendency towards erythrocyte aggregation by increasing the CAMP (cyclic adenosinmonophosphate) by inhibiting the phosphodiesterase thereby producing a decrease in the viscosity of the blood. In addition, the thrombocytes or platelet aggregation is reduced and the fibrinogin and plasma viscosity lowered. R. Muller, Therapiewoche 30, 2440-2451 (1980); Aviado, Porter, Pharmacotheraphy Vol. 4, No. 6 (1985); Dettelbach, Aviado, Journ. of Clin. Pharm. 1985, pages 8-26.